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Parasitology > GI Nematodes > Flashcards

GI Nematodes Flashcards

1
Q

How would you treat a low risk dog for nematodes?

A

generally based on fecal samples

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2
Q

What are the gastrointestinal nematodes?

A
  1. hookworm
  2. whipworm
  3. threadworm
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3
Q

Where do GI hookworms live?

A

small intestine

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4
Q

What are 3 types of hookworms?

A
  • Ancylostoma caninum - Ca (zoonotic)
  • Ancylostoma tubaeforme - Fe (may not be zoonotic b/c they bury their poo)
  • Uncinaria stenocephala - Ca
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5
Q

What are the defining features of adult Uncinaria stenocephala?

A
  • prominent buccal capsule, opening into which has 2 cutting plates, 1 on each side of its ventral aspect
  • exact struct of buccal capsule is important in distinguishing btwn various hookworm spp
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6
Q

What are the defining features of Uncinaria stenocephala eggs?

A
  • oval w/ a thin smooth shell
  • when freshly passed, each egg contains a few cells grouped together - a morula (strongyle type egg)
  • eggs are slightly larger than those of Ancylostoma caninum, & this is basis for differentiation of 2 parasites on fecal exams
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7
Q

What is the host range & geographic distribution of Uncinaria stenocephala?

A
  • common in Ca & other canids
  • rare in Fe & other felids
  • in cooler areas of the world (including N. Canada)
  • relatively common in arctic fox, red fox, coyote, & wolves in Canada
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8
Q

what is the life cycles of Uncinaria stenocephala?

A
  • direct
  • eggs are passed in feces of Ca DH
  • in enviro, L1 develops in each egg
  • larva then hatches
  • devs into infective L3 (w/in 4-8 days under ideal conditions - temps > 7.5 C)
  • Ca generally become infected by ingestion of infective larvae (followed by mucosal migration)
  • infective larvae can penetrate the skin, but only v rarely dev into adults in intestine
  • Ca can also become infected by ingesting L3 in tissues of sm mammal paratenic hosts
  • their PPP is 2-3 wks
  • prenatal & transmammary infections are not thought to occur
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9
Q

What is the epidemiology of Uncinaria stenocephala?

A
  • eggs & larvae are more cold tolerant than those of Ancylostoma caninum (southern hookworm of canids)
  • enviro stages of hookworms are not particularly robust (compared to other parasites)
  • do best in warm, moist enviro conditions that support survival & rapid dev of infective larvae
  • sub-optimal hygiene also favours parasite by exposing susceptible Ca to these larvae
  • for animals in kennels or shelters, where host density enhances opportunities for transmission, effective treatments & maintaining clean enviro are key elements of all control programs
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10
Q

what is the pathology & clinical signs of Uncinaria stenocephala?

A
  • appears to be only mildly pathogenic, although large #s of adults plug-feeding in mucosa can cause protein losing enteropathy, mucousy diarrhea, & poor growth
  • although percutaneous invasion is rare dermatitis associated w/ infective larvae has been reported in Canada
  • adult animals w/ low intensity infections may be entirely subclinical
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11
Q

What is the public health significance of Uncinaria stenocephala?

A
  • not though to be significantly zoonotic
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12
Q

What are differential diagnoses for hookworm dermatitis caused by Uncinaria stenocephala?

A
  • allergy, mange, other nematodes (Ancylostoma, Pelodera)
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13
Q

How is Uncinaria stenocephala diagnosed?

A

fecal float, coproAg, larvae on skin scraping

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14
Q

how to treat/control for Uncinaria stenocephala?

A

control as for other hookworms (less serious)

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15
Q

Where does Ancylostoma caninum live in Ca?

A

small intestine

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16
Q

Defining features of adult Ancylostoma caninum?

A
  • prominent buccal capsule (opening to which has 3 pointed teeth on each side of its ventral aspect)
  • exact struct of buccal capsule is important in distinguishing btwn various hookworm spp
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17
Q

Defining features of Ancylostoma caninum eggs?

A
  • oval w/ thin smooth shell (typical strongyle type eggs)
  • when freshly passed, each egg contains a few cells grouped together - a morula
  • eggs are slightly smaller than those of Uncinaria stenocephala, & this is basis for differentiation of 2 from fecal exams
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18
Q

What is the host range & geographic distribution of Ancylostoma caninum?

A
  • occurs in Ca
  • occasionally in people
  • in warmer parts of world (including S. USA)
  • in Canada, is not common
  • most cases are in Ca from endemic areas outside country or from kennels where conditions support transmission
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19
Q

What is the life cycle of Ancylostoma caninum?

A
  • live in sm intestines
  • eggs are passed in feces
  • in enviro, L1 develops w/in each egg
  • larva then hatches & devs into infective 3rd stage (w/in 5-8 days under ideal conditions - temps > 15 C)
  • Ca are infected when larvae are ingested or penetrate skin
  • following ingestion, in pups < 6m of age, most larvae follow mucosal migration
  • in young or naive Ca, infective larvae that penetrate skin follow SEMI-TRACHEAL MIGRATION (sub q tissues -> vasculature -> R heart -> lungs -> trachea -> pharynx -> GI tract)
  • PPP is 2-3 wks, shorter in pups
  • in Ca older than 6m, larvae acquired through ingestion or through skin increasingly undergo somatic migration (following ingestion, GI tract -> portal vessels -> liver -> R heart -> lungs -> L heart -> somatic tissue)
  • OR following skin penetration, Sub q tissues -> vasculature -> R heart -> lungs -> L heart -> somatic tissue
  • in female dogs, these larvae in the tissues can become mobilized during late pregnancy & travel to mammary glands where they infect nursing pups through colostrum & milk for @ least 1st 3 wks of lactation
  • this transmammary transmission is most important source of exposure for young pups (in which L3 larvae ingested in milk undergo mucosal migration
  • single massive infection of breeding female may infect multiple litters
  • finally, dogs may become infected by ingestion of L3 in range of paratenic hosts
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20
Q

What is the epidemiology of Ancylostoma caninum?

A
  • exposure generates immunity which is, however, not totally protective
  • thus, while in general parasite has a higher prevalence & intensity in younger animals, heavy burdens can also be seen in adult Ca
  • in areas where hookworm disease is endemic, transmammary transmission is often v significant means of maintaining parasite
  • enviro stages of hookworms are not particularly robust (compared to other parasites)
  • do best in warm, moist enviro conditions that support dev & survival of infective larvae
  • sub-optimal hygiene also favours parasite by exposing susceptible dogs to these larvae
  • for animals in kennels & shelters, where host density enhances opportunities for transmission, effective treatments & maintaining clean enviro are key elements of all control programs
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21
Q

What is the pathology & clinical signs of Ancylostoma caninum?

A
  • infective larvae penetrating skin may cause localized lesions - cutaneous larva migrans - which is most common in areas of body in contact w/ ground (ventral dermatitis)
  • pre-adults & adults in intestines suck blood, which in heavy infections, can cause severe even fatal anemia esp. in untreated young pups
  • pre-adult & adult parasites attach to intestinal mucosa using their buccal capsule, abrade host tissues w/ their teeth, & secrete anti-coagulant
  • they suck blood v rapidly & they graze - feed for a while in 1 site, then detach leaving site bleeding, then re-attach in new location
  • initially normocytic, normochromic anemia -> progresses to hypochromic, microcytic
  • clinical signs of hookworm disease are primarily those associated w/ blood loss anemia although migrating larvae can cause respiratory signs in heavily infected pups
  • infection is more common than is clinical disease, & some adult dogs can harbour sm or moderate burdens w/ few obvious adverse effects
  • in Ca of any age, other concurrent disease may exacerbate effects of hookworm infection
  • in people: cutaneous larval migrans & eosinophilic enterocolitis (sub-adults in SI)
  • cutaneous larval migrans can be seen in skin as creeping eruptions, serpentine, red, itchy tracts, occupational hazard for those who work w/ soil in warm regions
22
Q

What are the 4 clinical syndromes?

A
  1. per-acute (nursing pups in second week of life, severe anemia in PPP, melena, death)
  2. acute (older pups exposed to high infective doses, severe anemia in PPP)
  3. chronic compensated (adult dogs in endemic areas, no or few clinical signs)
  4. secondary decompensated (adult Ca w/ concomitant health/immunity probs)
23
Q

How is Ancylostoma caninum diagnosed?

A
  • based on hx & clinical signs
  • coproAg (even during PPP)
  • fecal float - strongyle type egg
  • adult nematode ID
24
Q

How do we control for Ancylostoma caninum?

A
  • deworm pups (& kittens) starting @ 2 wks old (Benximidazoles, macrocyclic lactones)
  • supportive therapy (transfusion); hand raise pups if necessary
  • extra label treatment of pregnant & lactating females
  • spay females
  • enviro hygiene & kennel management
  • treatment failures & multi drug resistance is increasingly common in USA & Canada
  • larval leak: repopulation of gut from somatic pool following treatment
25
Q

What are the 2 possible outcomes of L3 hookworm larvae after entering Ca?

A
  1. DEVELOPMENT (maturing into reproductively active adult worm in small intestine)
    - mature females may produce 2000-16000 eggs/day
  2. ARRESTED DEVELOPMENT (remaining dormant in the tissues)
    - not killed by dewormers
    - NOT DETECTED BY FECAL TESTS
    - can survive for yrs
    - CAN RESUME DEV (DURING PREGNANCY OR “LARVAL LEAK”)
26
Q

What is the public health significance of Ancylostoma caninum?

A
  • people can dev cutaneous larvae migrans associated w/ invasion by infective larvae (often from laying on contaminated beach or through occupational exposure to soil)
  • v rarely, infective larvae dev to adults in human GI tract & cause eosinophilic enteritis (not blood loss)
  • people are considered aberrant DH in which parasite does not generally complete its life cycle
27
Q

what are the defining features of adult Ancylostoma tubaeforme?

A
  • basically similar in structure to Ancylostoma caninum, w/ 3 prs of pointed teeth arising from dorsal margin of buccal capsule
28
Q

What are the defining features of Ancylostoma tubaeforme eggs?

A
  • similar to Ancylostoma caninum but slightly longer
29
Q

What is the life cycle of Ancylostoma tubaeforme?

A
  • direct
  • Fe may become infected through ingestion/skin penetration of L3 in enviro (subsequently following mucosal or semi-tracheal migration routes, respectively) or ingestion of L3 in paratenic hosts (subsequently following mucosal migration)
  • relative importance of these transmission routes is not known
  • PPP is 2-4 wks
  • there is no evidence of prenatal or transmammary transmission
30
Q

facts about Ancylostoma tubaeforme:

A
  • rare in Fe in Canada, more common in USA
  • life cycle similar to Uncinaria - no somatic larvae or transmammary transmission
  • can be asymptomatic
  • can cause anemia, diarrhea (melena), & weight loss in kittens
  • considered potentially zoonotic
31
Q

What is the public health significance of Ancylostoma tubaeforme?

A
  • isnt considered significant zoonosis
  • in theory it would be possible for infective larvae to invade human skin, but burying of feces by Fe & use of litter boxes probably minimize this risk
32
Q

Where do threadworms live in dogs?

A

small intestine

33
Q

What threadworm sp do we care about?

A

Strongyloides stercoralis

34
Q

What is the defining features of adult Strongyloides stercoralis?

A
  • parasitic adults are all female
  • v sm, cannot easily be seen w/o microscope
  • pharynx occupies almost half of total length of nematode
35
Q

What is the defining features of Strongyloides stercoralis rhabditiform larvae?

A
  • eggs hatch in intestinal lumen & this larvae is passed in feces
  • rhabditiform pharynx
36
Q

What is the lifecycle of Strongyloides stercoralis?

A
  • adult females are located deep in mucosa of sm intestine
  • these females repro by parthenogenesis (producing both male & female offspring)
  • eggs hatch in GI tract
  • L1 (rhabditiform larvae) are passed in feces
  • male L1 proceed to become free-living adult males
  • female larvae can either moult twice, developing into infective L3 larvae or moult two more times & dev into free-living adult females
  • free-living adults mate once & produce female rhabditiform larvae which dev into infective L3
  • translation from L1 to L3 can occur rapidly (in a matter of days)
  • infection of dog follows skin penetration by or ingestion of L3 females
  • in Ca, these larvae migrate in vasculature through liver & lungs, where they break out from branches of pulmonary artery into airways, are coughed up & swallowed, & move into small intestine (where they complete their dev into adult females)
  • PPP is 7 - 14 days
  • prenatal inf of pups do not occur, but transmammary inf occurs in females infected immediately post-partum
  • in people, & perhaps in Ca, it is capable of auto-infection, where rhabditiform larvae become infective larvae (due to rapid translation ( either in intestinal lumen or in peri-anal area)
  • in people, particularly those who are immunocompromised, autoinfection can result in lrg or v persistent infections
37
Q

What is the pathogenesis of Strongyloides stercoralis?

A
  • diarrhea
  • resp signs
  • cutaneous larval migrans (people) -> visible meandering lesion associated w/ migrating larvae (similar lesions can be produced by larvae of human & canine hookworm)
  • chronic bouts of abdominal pain & diarrhea esp in immunosuppressed Ca/ people (autoinfection)
  • eosinophilic enterocolitis
38
Q

How is Strongyloides stercoralis diagnosed?

A
  • larvae detected in Baermann on fresh feces
  • in older feces, must distinguish from free living larvae & from hatched hookworm larvae
39
Q

How do we control for Strongyloides stercoralis?

A
  • extra label macrocyclic lactones
  • environmental hygiene
40
Q

What is the epidemiology/ecology of Strongyloides stercoralis?

A
  • distribution: worldwide, warm & humid places, South America, South Asia, Africa (not endemic in Canada)
  • people & dogs (cats?) are definitive hosts
  • free-living & parasitic cycles
  • transmammary transmission (larvae is acquired by dam during lactation)
  • internal & external autoinfection in immunocompromised hosts (severe disease)
41
Q

What is the public health significance of Strongyloides stercoralis?

A
  • zoonotic
  • can be transmitted from Ca to people & vice versa
  • in human host, larvae can cause cutaneous larval migrans as they penetrate skin
  • v lrg burdens of migrating larvae can cause significant lung pathology
  • adult female can be associated w/ GI symptoms
  • particular prob in people who are immunosuppressed, in part b/c of auto-infection
  • parasite is a potentially v serious pathogen in these individuals
42
Q

Where do whipworms live?

A

large intestine

43
Q

Two types of whipworms ?

A
  • Trichuris vulpis (Ca)
  • Trichuris serrata (Fe)
44
Q

Which end is the skinny end in whipworms?

A

head

45
Q

definitive characteristic of Trichuris vulpis?

A
  • polar plug at each end
  • commonly described as lemon shaped
46
Q

life cycle of Trichuris vulpis?

A
  • live in caecum (w/ anterior ends “threaded” into mucosa
  • eggs are passed in feces
  • larvate in enviro in 10 days under optimal conditions (warm & wet)
  • usually, L1 are infective stage
  • infection follows ingestion of larvated eggs (containing L1) which hatch in intestinal lumen (releasing larvae that undergo mucosal migration & 4 moults to become adults)
  • PPP is relatively long (approx 3 m)
47
Q

how do you diagnose Trichuris vulpis?

A
  • fecal float (high specific gravity > or = 1.3)
  • COPROAG (works in PPP), CoporPCR
  • adult ID
48
Q

what is the pathogenesis of Trichuris vulpis?

A
  • adults suck blood
  • chronic colitis (bloody mucoid diarrhea)
49
Q

How do we control for Trichuris vulpis?

A
  • benximidazoles, macrocyclic lactones
  • treatment may need to be repeated several times do to long PPP
  • environmental hygiene (esp. shelters)
50
Q

What is the epidemiology & ecology of Trichuris vulpis?

A
  • worldwide distribution
  • canid definitive hosts (cats have own spp)
  • not considered mainstream zoonoses
  • direct, simple life cycle
  • long PPP
  • eggs are environmentally resistant
51
Q

What is the public health significance of Trichuris vulpis?

A
  • people have their own sp of whipworm (mjr cause of human morbidity in several areas of world)
  • v rarely zoonotic

Parasitology (13 decks)

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